Physiology and Pathophysiology of The Heart: Hemodynamic Cycle, Heart Sounds, Valvular Heart Disorders

Physiology and Pathophysiology of the heart
Part 1
Hemodynamic cycle, heart sounds,

valvular heart disorders
1 2 3
Phase
4 5 6
Aortic
Pressure
120
Press 80
(mmHg)
A
RA
LV Press
40
LA
PA
LA Press
v
0
LVEDV
120
LV
RV
LV
Vol
(ml)
80
LVESV
40
ECG
Phase 1
Atrial Contraction
IV
Heart
Sounds
II
III
0.4
Time (sec)
0.8
1 2 3
Phase
4 5 6
Aortic
Pressure
120
Press 80
(mmHg)
A
RA
LV Press
40
LA
PA
LA Press
v
LV
RV
LVEDV
120
LV
Vol
(ml)
80
LVESV
40
ECG
Phase 2
Isovolumetric
Contraction
IV
Heart
Sounds
II
III
0.4
Time (sec)
0.8
1 2 3
Phase
4 5 6
Aortic
Pressure
120
Press 80
(mmHg)
A
RA
LV Press
40
LA
PA
LA Press
v
0
LVEDV
120
LV
RV
LV
Vol
(ml)
80
LVESV
40
ECG
Phase 3
Rapid Ejection
IV
Heart
Sounds
II
III
0.4
Time (sec)
0.8
1 2 3
Phase
4 5 6
Aortic
Pressure
120
Press 80
(mmHg)
A
RA
LV Press
40
LA
PA
LA Press
v
0
LVEDV
120
LV
RV
LV
Vol
(ml)
80
LVESV
40
ECG
Phase 4
Reduced Ejection
IV
Heart
Sounds
II
III
0.4
Time (sec)
0.8
1 2 3
Phase
4 5 6
Aortic
Pressure
120
Press 80
(mmHg)
A
RA
LV Press
40
LA
PA
LA Press
v
LV
RV
LVEDV
120
LV
Vol
(ml)
80
LVESV
40
ECG
Phase 5
Isovolumetric
Relaxation
IV
Heart
Sounds
II
III
0.4
Time (sec)
0.8
1 2 3
Phase
4 5 6
Aortic
Pressure
120
Press 80
(mmHg)
A
RA
LV Press
40
LA
PA
LA Press
v
0
LVEDV
120
LV
RV
LV
Vol
(ml)
80
LVESV
40
ECG
Phase 6
Rapid Filling
IV
Heart
Sounds
II
III
0.4
Time (sec)
0.8
HR 75/MIN
HR 200/MIN Skeletal muscle
Hemodynamic cycle duration
0,80
0,30
Systole
0,27
0,16
Action potential duration
0,25
0,15
0,005
Absolute refraction period
0,20
0,13
0,004
Relative refraction period
0,05
0,02
0,003
Diastole
0,53
0,14
Heart sounds
Heart sounds
Sound Appears during
S1
S2
S3
S4
Results from:
Caused by the sudden block of
Isovolumetric
reverse blood flow due to closure
contraction
of the atrioventricular valves
Caused by the sudden block of
Isovolumetric
reversing blood flow due to closure
relaxation
of the semilunar valves
Physiology (benign) in children,
also trained individual and
sometimes in pregnancy;
Rapid ventricle filling protodiastolic gallop, ventricular
gallop
Pathology failing left ventricle
(dilated ventricle)
Atrial systole
Low plasticity of the ventricles (ex.

Hypetrophy)
presystolic gallop or atrial gallop
Heart sounds murmurs
Cardiac output
Cardiac Output = Heart Rate (HR) x Stroke Volume (SV)

HR regulation
SV regulation
HR regulation
www.cvphysiology.com
ANS and regulation of the heart work

Vagal nerve
Sympathetic system
SA
AV
ACh
Muscarinic M2 rec
activation
NE
Adrenergic 1 rec
activation
+
HR
Inotropy
Na+
Ca2+
Ca2+
Na+
Na+
Na+
Ca2+
Ca2+
Na+
Na+
Ca2+
Na+
Ca2+
Na+
Ca2+
NA
Na+
Na+
Ca2+
Gs
cAMP
cAMP
Gs
Na+
Ca2+
Ca2+
Na+
Ca2+
NA
Na+
Na+
Ca2+
Ca2+
Na+
Na+
Ca2+
Na+
Na+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
NA
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Gs
cAMP
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Sarcoplasmic reticulum
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
cAMP
Gs
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
NA
Ca2+
Ca2+
K+
Na+
K+
digoxin
Na+
K+
Na+
Na+
K+
Na+
Na+
Na+
5%
15%
Na+
K+
Na+
ATP
Ca2+
ATP
Na+/Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Na+
Na+
Ca2+
Na+
Ca2+
Ca2+
Ca2+
Na+
Ca2+
Ca2+
Ca2+
Na+
Ca2+
ATP
80%
Sarcoplasmic reticulum
ATP
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
Ca2+
NA
Ca2+
Ca2+
Na+
Ca2+
Ca2+
Na+
Ca2+
Na+
ACh
M
+
+
+
-
+
-
+
-
Gi
Na+
Na+
+
-
+
+
-
cAMP
K+
K+
K+
K+
K+
K+
K+
K+
cAMP
Na+
Na+
Na+
Ca2+
Ca2+
K+
Na+
Ca2+
Ca2+
Na+
K+
K+
K+
Na+
K+
K+
+
-
K+
K+
+
-
K+
K+
+
-
Gi
M
ACh
FRANK-STARLING LAW
Decreased afterload
Increased afterload
preload
What affects preload?
FRANK-STARLING LAW - Contractility
Decreased contractilty
Increased contractility
preload
Contraction regulation
HOMEOMETRIC regulation depends on contractility
HETEROMETRIC regulation depends on Frank-Starling mechanism
Anrep effect wzrost kurczliwoci w odpowiedzi na gwatowny wzrost afterload

Bowditch effect depends on HR increase
Contractility
Clinical index for inotropy evaluation:
Ejection Fraction (EF) = SV/EDV * 100%
dP/dt
Stroke volume regulation
Case 1
62-years old women with history of atrial
fibrillation
shortness of breath, when she lies down flat in

the supine position,
nocturia,
she has run out of digoxin, which she took to

control her heart rate
Case 1
bood pressure 90/65 mm Hg,

irregular heart rate ~ 120/min,
pulmonary rales,
increased jugular venous distension,

peripheral edema of legs
the primary diagnosis
the primary diagnosis
atrial fibrillation
congestive heart failure
Question 1:
What can be a cause of atrial fibrillation in this

patient?
Answer 1:
the run out of digoxin
Question 2:
What is the mechanism of digoxine in the heart?
the positive inotropic effect

the negative chrono- dromotropic effect
Why?
The sodium/potassium pomp inhibition

in cardiomiocytes membrane
Question 3:
What factors affect stroke volume?
Answer 3:
Contractility
Preload
Afterload
Which of above factors was changed during atrial
fibrillation?
Question 4:
How does stimulation of muscarine receptors affect

contractillity?
Answer 4:
stimulation of muscarinic receptors decreases

contractility only in atria
Case 2
25-year old pregnant women
no medication,
no complications with this pregnancy

she was admitted to the hospital in active
phase of labor
she asked for pain relief
Case 2
the epidural nerve block has been done
dizzines
low blood pressure

raid heart rate
Case 2
intravenous fluid bolus and a small amount
of ephedrine were recommended
the lack of sympthoms
Question 1:
Why would epidural analgesia cause these

sympthms?
Answer 1:
sympathetic blockade (T10 L3) resulting in

decreased venous pressure and thus decreased
cardiac output and decreased pheripheral

resistance resulting in hypotension
Question 2:
How would ephedrine (IV) counter the hypotension?
Answer 2:
ephedrine increases 1 stimulation, leading to

contraction of the venous musculature,
increasing VP, and thus CO and pheripheral

resistance
Cardiac Output in relation

to venous pressure
Case 3
62-year old man
10-year history of arterial hypertension and dyslipidemia;
Since couple moths lack tolerance for physical effort (he cant
climb up to the 2nd floor) and several times he reported angina
pectoris
Admitted to a Cardiology Unit after syncope with arising

dyspnoe;
Physical examination:
HR 123/min
Heart gallop
Loud heart murmur in the aortic area

Blood congestion in pulmonary circulation;
LV
hypetrophy
Calcificated
aortic valve
Turbulent blood
flow through LV
outflow
Clinical questions:
1. What should be diagnosed in our patient?

2. Why systolic murmur in the aortic area?
3. Why patient developed heart failure?

4. Why in the echocardiography LV hypertrophy was
observed?
5. Why patient developed symptoms of the ischaemia?
Clinical questions:
1. What should be diagnosed in our patient?

Severe symptomatic aortic stenosis complicated with
acute heart failure.
Clinical questions:
1. Why systolic murmur appeared in the aortic area?

Sytolic aortic murmur appeared when blood was ejected from
LV through narrow aortic valve.
Clinical questions:
1. Why patient developed heart failure?

Blood stasis in LV according to the narrowing of aortic
valve resulted in the volume and pressure overload of the

LV (LVEDP) -> and LA.
Increased left atrium pressure decreased venous return from

pulmonary circulation what resulted in pulmonary
congestion.
Clinical questions:
1. Why in the echocardiography LV hypertrophy was

observed?
During development of the aortic stenosis afterload gradually

increased. A rise in afterload increased duration of a isovolumetric
systole.
Clinical questions:
1. Why patient developed symptoms of the ischaemia?

Cardiac muscle hypertrophy -> higher metabolic
demand (higher O2 demand).

Higher afterload -> lower stroke volume
Low SV -> low BP

Low coronary perfusion
Low SV -> higher HR -> lower left coronary perfusion

Physiology and Pathophysiology of The Heart: Hemodynamic Cycle, Heart Sounds, Valvular Heart Disorders

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Physiology and Pathophysiology of The Heart: Hemodynamic Cycle, Heart Sounds, Valvular Heart Disorders

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Physiology and Pathophysiology of the heart

Hemodynamic cycle, heart sounds,

HR 200/MIN Skeletal muscle

Hemodynamic cycle duration

Action potential duration

Absolute refraction period

Relative refraction period

Low plasticity of the ventricles (ex.

Heart sounds murmurs

Cardiac Output = Heart Rate (HR) x Stroke Volume (SV)

ANS and regulation of the heart work

What affects preload?

FRANK-STARLING LAW - Contractility

HETEROMETRIC regulation depends on Frank-Starling mechanism

Anrep effect wzrost kurczliwoci w odpowiedzi na gwatowny wzrost afterload

Clinical index for inotropy evaluation:

Ejection Fraction (EF) = SV/EDV * 100%

Stroke volume regulation

shortness of breath, when she lies down flat in

she has run out of digoxin, which she took to

bood pressure 90/65 mm Hg,

increased jugular venous distension,

the primary diagnosis

the primary diagnosis

congestive heart failure

What can be a cause of atrial fibrillation in this

the run out of digoxin

What is the mechanism of digoxine in the heart?

the positive inotropic effect

The sodium/potassium pomp inhibition

What factors affect stroke volume?

How does stimulation of muscarine receptors affect

stimulation of muscarinic receptors decreases

no complications with this pregnancy

she asked for pain relief

low blood pressure

the lack of sympthoms

Why would epidural analgesia cause these

sympathetic blockade (T10 L3) resulting in

cardiac output and decreased pheripheral

How would ephedrine (IV) counter the hypotension?

ephedrine increases 1 stimulation, leading to

increasing VP, and thus CO and pheripheral

Cardiac Output in relation

62-year old man

10-year history of arterial hypertension and dyslipidemia;

Admitted to a Cardiology Unit after syncope with arising

Loud heart murmur in the aortic area

1. What should be diagnosed in our patient?

3. Why patient developed heart failure?

1. What should be diagnosed in our patient?

acute heart failure.

1. Why systolic murmur appeared in the aortic area?

LV through narrow aortic valve.

1. Why patient developed heart failure?

valve resulted in the volume and pressure overload of the

Increased left atrium pressure decreased venous return from

1. Why in the echocardiography LV hypertrophy was

During development of the aortic stenosis afterload gradually

1. Why patient developed symptoms of the ischaemia?

demand (higher O2 demand).

Low SV -> low BP

Low SV -> higher HR -> lower left coronary perfusion